Key result
Pediatric blood cardioplegia is linked to a ~44% rise in hsp70-1 expression correlating with cross-clamp time.
Why the study?
Up-regulation of the inducible isoform HSP70-1 reduces myocardial cell damage during open-heart surgery and appears protective against ischemia, prompting assessment of its gene expression during blood cardioplegic arrest in children undergoing congenital heart defect repair.
Does blood cardioplegia induce hsp70-1 gene expression in pediatric patients undergoing congenital heart surgery?
Observational (n=59)
Does blood cardioplegia induce hsp70-1 gene expression in pediatric patients undergoing congenital heart surgery?
Blood cardioplegia induces an increase in hsp70-1 gene expression that correlates with aortic cross-clamp time, supporting its protective role against ischemia/reperfusion injury in pediatric heart surgery.
Hsp70-1 induction by blood cardioplegia may mark ischemia protection in pediatric cases; hypothesis-generating and should not yet change practice.
BACKGROUND: In response to many stress stimuli, cardiomyocytes produce a common set of heat shock proteins (HSP). Up-regulation of HSP70-1 (the inducible isoform) is known to reduce the risk of myocardial cell damage during open-heart surgery and seems to be protective against ischemia. We assessed hsp70-1 gene expression during blood cardioplegic arrest in children undergoing surgical correction of congenital heart defects. METHODS: In tissue samples taken from the right atrium of 59 pediatric patients, we examined hsp70-1 gene expression using a real-time quantitative reverse transcription PCR, with 18S rRNA as internal standard. RESULTS: On average, hsp70-1 gene expression was higher than the baseline level by a factor of 1.44+/- 0.17 (mean+/-SEM). A significant relationship between hsp70-1 mRNA levels and aortic cross-clamp time was observed (R(2)=0.069, p=0.044). Conversely, no significant correlation was observed between hsp70-1 mRNA levels and temperature. CONCLUSIONS: These data suggest that blood cardioplegia can induce an increment in the expression of hsp70-1, confirming its protective role in ischemia/reperfusion injury.
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Vittorini et al. (2007) conducted an observational in Congenital heart defects (n=59). Blood cardioplegic arrest vs. Baseline was evaluated on hsp70-1 gene expression. Blood cardioplegia during pediatric heart surgery induced a 1.44-fold increase in hsp70-1 gene expression, which significantly correlated with aortic cross-clamp time (P=0.044).
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